GPCR-Gs mediates the protective effects of ginsenoside Rb1 against oxygen-glucose deprivation/re-oxygenation-induced astrocyte injury
- Author:
Xi Wang
;
Ying Liu
;
Juan Li
;
Jiayu Xie
;
Yi Dai
;
Minke Tang
1
Author Information
1. tangmk@bucm.edu.cn
- Publication Type:期刊文章
- Keywords:
Ginseng;
Ginsenoside Rb1;
Receptor;
GPCR;
Astrocytes;
Neuroprotective effects
- From:
Journal of Traditional Chinese Medical Sciences
2024;11(1):33-43
- CountryChina
- Language:English
-
Abstract:
Objectives:To investigate whether the protective actions of ginsenoside Rb1 (Rb1) on astrocytes are mediated through the Gs-type G-protein-coupled receptor (GPCR-Gs).
Methods:Primary astrocyte cultures derived from neonatal mouse brain were used. Astrocyte injury was induced via oxygen-glucose deprivation/re-oxygenation (OGD/R). Cell morphology, viability, lactate dehydrogenase (LDH) leakage, apoptosis, glutamate uptake, and brain-derived neurotrophic factor (BDNF) secretion were assessed to gauge cell survival and functionality. Western blot was used to investigate the cyclic adenosine monophosphate (cAMP) and protein kinase B (Akt) signaling pathways. GPCR-Gs-specific inhibitors and molecular docking were used to identify target receptors.
Results:Rb1 at concentrations ranging from 0.8 to 5 μM did not significantly affect the viability, glutamate uptake, or BDNF secretion in normal astrocytes. OGD/R reduced astrocyte viability, increasing their LDH leakage and apoptosis rate. It also decreased glutamate uptake and BDNF secretion by these cells. Rb1 had protective effects of astrocytes challenged by OGD/R, by improving viability, reducing apoptosis, and enhancing glutamate uptake and BDNF secretion. Additionally, Rb1 activated the cAMP and Akt pathways in these cells. When the GPCR-Gs inhibitor NF449 was introduced, the protective effects of Rb1 completely disappeared, and its activation of cAMP and Akt signaling pathways was significantly inhibited.
Conclusion:Rb1 protects against astrocytes from OGD/R-induced injury through GPCR-Gs mediation.
